Showing papers by "Maria Rosa Chitolina Schetinger published in 1997"
TL;DR: 9-Amino-1,2,3,4-tetrahydroacridine, proposed as a drug for the treatment of Alzheimer's disease, can alter in vitro ATP degradation in synaptosomes from the central nervous system.
Abstract: 1. 9-Amino-1,2,3,4-tetrahydroacridine (THA), an acetylcholinesterase inhibitor, significantly inhibited in vitro the ATP diphosphohydrolase activity of synaptosomes from the cerebral cortex and hippocampus of adult rats. 2. THA did not inhibit in vitro the 5'-nucleotidase activity of synaptosomes from cerebral cortex and hippocampus of rats. 3. THA exerted an uncompetitive inhibition on ATP diphosphohydrolase activity. This mechanism of inhibition was the same in the 2 different synaptosomal fractions (cerebral cortex and hippocampus) studied. 4. THA, proposed as a drug for the treatment of Alzheimer's disease, can alter in vitro ATP degradation in synaptosomes from the central nervous system.
5 citations
01 Jan 1997
TL;DR: The hippocampus is a classical predeliction site for ischemic injury of the selective vulnerability type3, which can produce necrosis of neurons, glia, and other supportive brain cells.
Abstract: Ischemic brain injury produced by stroke or cardiac arrest is a major cause of human neurological disability1. The molecular consequences of brain ischemia include changes in cell signalling (neurotransmitters, neuromodulators); in signal transduction (receptors, ion channels, second mesengers, phosphorylation reactions); in metabolism (carbohydrate, protein, fatty acid, free radicals); and in gene regulation and expression2. These abnormalities in cellular metabolism can produce necrosis of neurons, glia, and other supportive brain cells1, 2. Neurons differ in their intrinsic sensitivity to ischemic insults and in their ability to recover from such an impact3. The hippocampus is a classical predeliction site for ischemic injury of the selective vulnerability type3.
4 citations